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Indicates that they will present prelim data the 1st half of 2013 (at CROI) for SB-728-902-5 and SB-728-1101, with complete data by the end of 2013. They also indicate they will be Phase 3 "ready" in 2013.

Some fascinating and promising basic research and some disturbing presentations:

374 HIV Preferentially Infects Hematopoietic Progenitor Cells with High CD4 and Can Be Found in CD133+ Hematopoietic Progenitor Cells in a Subset of Optimally Treated People with Long-term Viral Suppression

This means that in some individuals the virus is not only in our bone marrows but in (I presume) unipotent "stem"cells, I if I were to guess within the lymphoid lineage which inclueds our T-Cells, both CD4 and CD8, B-cells and natural killer cells. However CD4 is also expressed on monocytes and macrophages too, and there is not enough information in the title to say which hematopoietic population the indentified cells belong to.

Bottom line is, as these progenitors grow up and divide any integrated virus goes along with them-another damn reservoir.

CD133, originally known as AC133.[1] CD133 is a glycoprotein also known in humans and rodents as Prominin 1 (PROM1).[2] Currently the function of CD133 is unknown. It is a member of pentaspan transmembrane glycoproteins (5-transmembrane, 5-TM), which specifically localize to cellular protrusions.

Regarding Phase II vs III for Sangamo. BASICALLY, Phase II figures out if something works, Phase III compares the product to something similar in the market. There is'nt anything to compare Zinc Fingers to. Yes, there will be a Phase III, but phase II is BIG for Sangamo..although something CAN go wrong in the post I phases.

Alas the CROI 2013 abstract on stem cell "infestation" is not the first paper on the subject. The above link doesn't take you to the abstract, but the title and the fact it is published in Nature would add weight, which these new results would confirm.

I should of remembered this study as it is on a site I go to periodically.

These were in CD34 cells, which acts as an adhesion molecule and binds CD62L or something called L-selectin. The receptor is found in precursors of hematopoietic cells, and endothelial cells in lymph glands.

Yeah it is damn confusing, for instance the text I reference often didn't have any information on this CD133 receptor (last edition 2012), whose function remains unknown. Without having access to the full paper one can't say with certainty what additional CD markers were present.

During Hemtopoises cells start out first as stem cells with universal potential, then advance to becoming multipotent followed by cells with unipotential before becoming the committed precursors and late differentiated and mature blood cells that we all know. The virus was found in what they call a unipotent lineage so my guess is this is downstream of actual stem cells with universal potential, which is a good thing as it narrows down which cell lineage harbors HIV.

As a bench researcher/lab supervisor I had trouble keeping up with what was going on the next bench. I knew a few physician scientists but they are a rare breed and if they are both, their families can suffer-as demanding as both jobs are. Our daughter is a physician.

I don't know if you saw an earlier comment that I made in one of the forums, but I'm schlepping Abul Abbas's text, "Cellular and Molecular Immunology," which you may have used. I started reading it in 1991 and I'm now reading the 7Th edition-and I still don't know a fraction of what I'd like to know.

Tadeys, check out my other thread on innate immune responses and the review I posted. I've got CD8's coming out my ears and I still haven't eradicated this bastard. I think any functional cure has got to involve tweaking our innate immune response, possibly by silencing integrated DNA through methylation. Of course it is tricky because HIV grabs and incorporates NFkb, a key transcription factor, into it's promoter region.